Allyloxy polyethoxy ether (APEO) and chloracetic acid were used to prepare allyloxy polyethoxy carboxylate (APEC). 8‐hydroxy‐1,3,6‐pyrenetrisulfonic acid trisodium salt was reacted with allyl chloride to produce fluorescent monomer 8‐allyloxy‐1,3,6‐pyrene trisulfonic acid trisodium salt (AP). APEC and AP were copolymerized with maleic anhydride (MA) to synthesize AP tagged no phosphate and nitrogen free calcium phosphate inhibitor MA‐APEC‐AP. Structures of AP, APEO, APEC, and MA‐APEC‐AP were carried out by FTIR and 1H‐NMR. Different MA : APEC mole ratios were employed for the manufacture of MA‐APEC‐AP to study the effect of mole ratio on performance of MA‐APEC‐AP. Relationship between MA‐APEC‐AP's fluorescent intensity and its dosage was studied. MA‐APEC‐AP's calcium phosphate inhibition was compared with the down to date calcium phosphate inhibitor (MA)‐ammonium allylpolyethoxy sulphate (APES). The results indicate that capability of MA‐APEC‐AP is heavily depended on the mole ratio of MA : APEC. Correlation coefficient r of MA‐APEC‐AP's fluorescent intensity and its dosage is 0.9983, and detection limit of MA‐APEC‐AP is 2.03 mg L−1. MA‐APEC‐AP can be used to accurately measure polymer consumption on line besides providing excellent calcium phosphate inhibition. © 2009 Wiley Periodicals, Inc. J Appl Polym Sci, 2009

Background: Recently, studies have demonstrated that microRNA-497 (miR-497) plays an important role in modulating tumor cell sensitivity to chemotherapeutic drugs; however, its role in cellular resistance to the effects of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) in treatment of nonsmall cell lung cancer (NSCLC) is not fully understood. In this study, we explored the potential of miR-497 in targeting the insulin-like growth factor-1 receptor (IGF-1R) signaling pathways to overcome gefitinib resistance. Methods: A gefitinib resistant human lung adenocarcinoma A549 cell line (A549/GR) was established by the method of gefitinib mutagenesis culture. Next, the A549/GR cells were transfected with miR-497 mimics to establish an miR-497 overexpression model, designated A549/GR-miR497-mimic. MTT assay was used to assess cell resistance to gefitinib, and western blot assay was employed to evaluate alterations of IGF-1R and the AKT1 signaling pathway. Results: We found that A549/GR-miR497-mimic cells (IC50 =33.76±0.97 μmol/L) were more sensitive to gefitinib than the control group (P<0.01). In addition, the expression levels of IGF-1R and phosphorylated AKT1 (p-AKT1) in A549/GR-miR497-mimic cells were reduced. Conclusions: We demonstrated that miR-497 may have the effect of reversing gefitinib resistance and increasing the sensitivity of NSCLC cells to EGFR-TKIs by inhibiting the expression of IGF-1R and reducing activation of the downstream AKT signaling pathway. Thus, miR-497 plays a vital role in the acquired resistance to EGFR-TKIs, and it may represent a potential therapeutic strategy to treat NSCLC exhibiting resistance to EGFR-TKIs.

Nasopharyngeal carcinoma (NPC) is a common cancer in southern China and Southeast Asia. Nowadays, radiotherapy is the therapy of choice for NPC patients, and chemotherapy has been found as an alternative treatment for advanced NPC patients. However, finding novel drugs and pharmacologically therapeutic targets for NPC patients is still urgent and beneficial. Our study showed that BIX-01294 (BIX) can induce autophagic vacuoles formation and conversion of LC3B-I to LC3B-II in NPC cells in both dose- and time-dependent manners. Notably, the combination of BIX and chemotherapeutic drugs significantly decreased the cell viability and increased the lactate dehydrogenase release. Meanwhile, BIX plus cis-platinum (Cis) treatment induced pyroptosis in NPC cells as featured by cell swelling and bubble blowing from the plasma membrane, the increased frequency of annexin V and propidium iodide (PI) double-positive cells, as well as the cleavage of gasdermin E (GSDME) and caspase-3. Moreover, the deficiency of GSDME completely shifted pyroptosis to apoptosis. Furthermore, the inhibition of autophagy by chloroquine and the knockout of ATG5 gene significantly blocked the BIX-induced autophagy as well as pyroptosis in both in vitro and in vivo studies. Our data demonstrated that BIX-combined chemotherapeutic drugs could induce the Bax/caspase-3/GSDME-mediated pyroptosis through the activation of autophagy to enhance the chemosensitivity in NPC.

Objective: To clarify the outcomes of elderly patients with COVID-19.Methods: All 265 confirmed adult patients with COVID-19 were included in this retrospective study, 43 (16.2%) of whom were 65 years and older. Electronic medical records of the subjects were reviewed to obtain information on clinical characteristics and outcomes. The allocations of medical resource were also recorded.Results: Only one death case occurred in the elderly. The mortality of elderly patients was no higher than that of young patients (2.3% vs. 0%, P = 0.126). The cure rate was 95.3% in elderly patients and 99.5% in young patients (P = 0.067), and the duration of hospitalization is 27 days in elderly patients and 18 days in young patients (P = 0.001). The elderly suffered from more comorbidities (67.4% vs. 24.8%, P < 0.001), most of which is hypertension. Significantly more severe cases occurred in elderly patients compared with young patients (37.2% vs. 16.7%, P = 0.004). The elderly were more likely to present with complications including acute respiratory distress syndrome, acute myocardial injury, septic shock and acute kidney injury (all P < 0.05), respectively. No medical staffs were infected during the treatment of COVID-19.Conclusion: The cure rate and the mortality of the elderly seemed to be no worse than that of the young, though the elderly were with longer hospitalization. Elderly patients with COVID-19 could be treatable if handled properly. More severe cases and complications in elderly patients should prompt for more complex treatment and special considerations.